RESUMEN
Lidocaine, a use-dependent Na(+) channel blocker, paradoxically evokes neural activation in the slowly adapting stretch receptor organ of crayfish at 5-10 mmol/l concentration. For elucidating the underlying mechanisms of this paradoxical effect, a series of conventional electrophysiological experiments were performed in the stretch receptor neurons of crayfish. In the presence of tetrodotoxin, lidocaine did not evoke impulse activity, however, a slowly developing and dose-dependent depolarization occurred in both the rapidly and slowly adapting stretch receptors. Similar effects were observed by perfusion of equivalent concentrations of benzocaine but not of procaine or prilocaine. Lidocaine did not evoke neural activity in the rapidly adapting neuron which fires action potential(s) in response to rapid changes in membrane potential. Slowly developing mode of the depolarization indicated the reason why only depolarization but not action potential responses were observed in the rapidly adapting neuron. The depolarizing effect of lidocaine was independent from any ionic channel or exchanger system. However, lidocaine and benzocaine but not procaine and prilocaine evoked a dose-dependent alteration in the input resistance of the neuron. It was proposed that the principal mechanism of the effect could stem from a change in the physical properties of the neuronal membrane.
Asunto(s)
Potenciales de Acción/efectos de los fármacos , Electrofisiología , Lidocaína/farmacología , Mecanorreceptores/efectos de los fármacos , Neuronas/efectos de los fármacos , Potenciales de Acción/fisiología , Animales , Astacoidea , Benzocaína/farmacología , Relación Dosis-Respuesta a Droga , Mecanorreceptores/fisiología , Neuronas/fisiología , Técnicas de Placa-Clamp , Prilocaína/farmacología , Procaína/farmacologíaRESUMEN
BACKGROUND: Drains are usually left after thyroid surgery to prevent formation of hematoma and seroma in the thyroid bed. This prospective randomized clinical trial was conducted to evaluate the necessity of drainage after total thyroidectomy for benign thyroidal disorders. METHODS: The patients were assigned randomly into two groups (group 1: with suction drain, group 2: fibrin glue). In the study, operating time, postoperative pain, the total amount of intramuscular analgesic administration, hospital stay, complications (such as wound infection, seroma, bleeding, hematoma, recurrent laryngeal nerve palsy or hypoparathyroidism), were recorded. RESULTS: The drained group (group 1) consisted of 2 men and 48 women with a mean age of 47.76±11.22 years. The nondrained (plus fibrin sealant)( group 2) (comprised of 10 men and 40 women with a mean age of 44.72±11.32 years. There was no significant difference in the gender, age, hormonal status and histopathological results of the patients between the two groups (P=0.18, P=0.36, P=0.28 and P=0.40, respectively). The operations performed were total thyroidectomy in all patients. Twenty-five patients (50%) in the non-drained group did not need intramuscular analgesic, whereas 15 patients (30%) did not in the drained group (P=0.01). In addition, the mean amount of intramuscular analgesic requirement was significantly less in the non-drained group than in the drained group (P=0.02). The complication rates were similar between the two groups. One case of hematoma (2%), two cases of seroma (4%) and three cases of transient hypoparathyroidism (6%) occurred in the non-drained group, whereas one case of hematoma (2%), two cases of seroma (4%), two cases of wound infections (4%) and two cases of transient hypoparathyroidism (4%) occurred in the drained group (P=0.69). No patient needed surgical revision or re-operation for any complication and all complications were successfully managed conservatively. CONCLUSION: Routine drainage of thyroid bed following thyroid surgery may not be necessary. Not draining the wound results in lesser morbidity and decreased hospital stay.
RESUMEN
Obstructive jaundice is associated with high morbidity and mortality. Major complications such as pulmonary dysfunction, renal failure and sepsis are frequently encountered. Recent studies and observations suggest that the free oxygen radicals (FORs) produced in obstructive jaundice may play a significant role in the etiopathogenesis of acute renal failure (ARF). Thirty rats were divided into three groups, as sham, control and treatment groups containing 10 rats each. Laparatomy was performed on each animal in the control and treatment groups and common bile ducts were ligated. Common bile duct was observed but was not ligated for the rats in the sham group. Saline solution injection was begun on the first day of surgical procedure and repeated once a day during the following 5 days. The same procedure was performed with oxygen radical scavenger dimethyl sulfoxide (1.5 mg/kg/day i.p.) instead of saline in the treatment group. The rats were sacrificed on the 7th postoperative day. On the 7th postoperative day, the bilirubin, urea and creatinine levels of the control and treatment groups were significantly higher in comparison with the sham group (p < 0.01). Although there was no statistically significant difference between the bilirubin levels of the control and treatment groups (p > 0.05), the urea and creatinine levels in the treatment group were significantly lower (p < 0.01). On the 7th postoperative day, the erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels of the control and treatment groups were significantly lower than those of the sham group (p < 0.01), whereas renal and erythrocyte malondialdehyde (MDA) levels were significantly higher (p < 0.01). Although SOD and GSH-Px levels did not differ significantly between the treatment and control groups (p > 0.05), renal and erythrocyte MDA levels of the treatment group were significantly lower than those of the control group (p < 0.01). The histopathological scores were significantly higher in the control and treatment groups (p < 0.01); there was no significant difference between the control and treatment groups (p > 0.05). FORs seem to play a significant role in the etiopathogenesis of renal failure in obstructive jaundice. Antioxidant treatment may decrease oxidative damage due to FORs and may prevent renal failure.